View clinical trials related to Pulmonary Hypertension.
Filter by:Extremely preterm infants are at risk for developing bronchopulmonary dysplasia (BPD) and associated chronic pulmonary hypertension (PH), a consequence of altered pulmonary vasculature. This condition occurs in about 25% of babies with BPD, and the association grows with increasing BPD severity. Other risk factors have been described as well. Morbidity and mortality associated with prematurity and/or BPD increase significantly in the presence of PH. Thus, international guidelines encourage the use of standardized screening protocols for this condition. However, several questions regarding these recommendations are left unanswered, such as a clear definition for PH in this population. The research aim is to prospectively evaluate prevalence, risk factors and clinical course of PH in these children. The investigators aim to identify at-risk infants early on and ultimately improve survival making use of an early targeted intervention.
Patients with pulmonary hypertension will be randomized into two groups. One group will receive telerehabilitation sessions including upper and lower extremity strengthening exercises and breathing exercises. The other will me monitored routinely. Patients will be assessed by 6 minute walk test, emphasis-10 questionnaire for quality of life and muscle strength with hand-held dynamometer.
- To evaluate different echocardiographic indices in diagnosis and follow up of group 1 pulmonary hypertension. - To evaluate blood biomarkers (troponin, uric acid and micro RNA) in naïve group 1 pulmonary hypertension.
Exercise training in Pulmonary arterial hypertension in the setting of rehabilitation leads to an enormous improvement of functional state and haemodynamics. However the underlying mechanism is still unkown. It is assumed to be relied on Right ventricular contractile reserve, but this has never been proven with goldstandard PV-loop assessment. Our aim is to evaluate the mechanism leading to the increase in functional state and to evaluate the impact of exercise (acute and chronic) on right ventricular performance
To identify clinical, echocardiographic, and hemodynamic parameters which can predict persistent PH after PMC, and also to determine the impact of persistent PH on the clinical outcomes.
To evaluate feasibility of photoplethysmography (PPG) of pulmonary arteries in adults children and neonates and to compare normal controls to premature newborns suffering from patent ductus arteriosus and neonates suffering from pulmonary hypertension.
The purpose of this study is to evaluate the efficacy and safety of mirabegron (a B3 adrenergic receptor agonist) in patients with pulmonary hypertension secondary to heart failure by conducting a randomized multicenter phase II placebo-controlled clinical trial.
The trial is a pilot study performed in the NICU's at Oslo University Hospital and Haukeland University Hospital preparing a multi-center randomized, controlled unblinded cross-over study, comparing high frequency ventilation (HFV) with and without volume guarantee (VG).
Research design: This is a controled prospective study. Methodology: Patients with newly diagnosed and untreated OSA with total apnea-hypopnea index (AHI) >5/h, and control (AHI<5/h) will be recruited from the Long Beach VA sleep center. Controls are subjects without OSA or other sleep disorders and no sign of pulmonary hypertension based on echo. The investigators also measure pulmonary artery pressure by 2D Echo and exclude patient with any sign of left heart dysfunction. PH will be defined as RVSP > 35 mmHg or mean PA pressure>25 mmHg. The investigators will recruit subjects with and without PH and OSA in three separate groups: 1. group one : OSA+ PH, 2. group two: normal individual with no OSA and no PH, 3. group three: OSA with no PH Pulmonary function test will be done to exclude patients with underlying lung disease. The inclusion criteria is: Age >20, AHI >5, AHI <5 (as control), RVSP > 35 mmHg OR Mean PA pressure>25 mmHg, RVSP < 35 mmHg OR Mean PA pressure < 25 mmHg (as control). Subjects will be excluded if they had known peripheral vascular disease, liver disease, hemolytic anemia, inflammatory disease, active infection, or if they were pregnant, on therapy for OSA, on chronic steroid treatment, or younger than 20 years of age, patients with left heart failure (systolic or diastolic), patients are on PH medications including sildenafil, active smokers, COPD and asthma, active infection or inflammatory disease and collagen vascular disease. Nocturnal polysomnography will be performed and scored according to the American Academy of Sleep Medicine. Exhaled Carbon monoxide (CO) will be measured with a calibrated fuel cell type electrochemical device with sensor sensitivity of 1 ppm. The mean of three reproducible measurements will be recorded and corrected for ambient CO. Exhaled Nitric Oxide (NO) will be measured. At each testing session, at least three flow-regulated FENO measurements will be performed. The investigators will repeat 2D Echo and measurements of above factors after 3 months of CPAP treatment. The investigators also check patient's compliance with the treatment by downloading data off of their CPAP device. Each subject will be informed of the experimental procedures, which is approved by the Human Investigation Committee of the VA-Long Beach. Finding: The investigators hypothesize that HO pathway causing perturbation of pulmonary endothelial function by inhibition of nitric oxide. Clinical significance: OSA is associated with PH, but exact mechanism is not well known. In the past, I have shown that increased endogenous CO in the setting of elevated NO concentration is associated with endothelial dysfunction in patient with OSA. Therefore, the investigators sought to investigate the roles of HO and NO pathways in patients with OSA associated with PH. Impact/significance: It addresses a fundamental gap in our understanding of how OSA results in increase the pulmonary artery pressure and if substantiated, will provide the basis for the design and testing of new approaches to prevention and treatment of OSA.
The mechanism governing how blood flows from the heart to the lungs depends on many factors including the pumping function of the right ventricle, properties of the arteries that carry the blood from the right ventricle to the lungs (pulmonary arteries), and the lungs themselves. Under normal conditions the pressure in the pulmonary arteries is well controlled and significantly lower than in the systemic circulation, however there are a number of conditions that lead to abnormally high pressures and significant morbidity and mortality. However different patients respond differently to similarly elevated pressures, leading doctors to believe that there must be differences in either the right ventricles, the properties of the arteries, or the lungs themselves. It can be difficult to determine the relative contributions of each of these factors on blood flow because their effects are superimposed on each other. One approach that has been used to look at this in other parts of the circulation (including in the systemic circulation and the coronary arteries) is to measure simultaneous pressure and flow, and apply a technique called wave intensity analysis (WIA). This technique can amongst other things, quantify the separate effects of wave reflection and the 'reservoir function' (or compliance) of the arteries, and in the systemic circulation WIA has increased the understanding of the mechanisms behind hypertension and the physiological changes of ageing. The pulmonary arteries are accepted to be very different from the systemic circulation and the mechanisms behind pulmonary hypertension are thought to be very different to those of systemic hypertension. This protocol aims to determine the major influences on blood flow in the pulmonary arteries in health and disease, to help to understand why some patients are affected more than others by elevated pulmonary pressures.